[1] PubMed ID: | 33475442 |
Disease Name: | Osteosarcoma |
Sample: | OS tissues |
Dysfunction Pattern: | Interaction(PTBP1/KHSRP ) |
Validated Method: | qRT-PCR//RIP |
Description: | Our data demonstrated HOTTIP was upregulated in OS tissues. In mechanism, PTBP1 and KHSRP highly expressed in OS and HOTTIP was identified to interact with PTBP1 to promote KHSRP expression. Meanwhile, we found that overexpression of KHSRP or PTBP1, individually, can partially remove the repression of HOTTIP suppression for OS cell progression. |
Causality: | Yes |
Causal Description: | HOTTIP knockdown resulted in a suppression of OS cell proliferation, invasion and migration, as well as a promotion of OS cell apoptosis, while HOTTIP overexpression exhibited opposite effects. |
Clinical-realted Application: | |
[2] PubMed ID: | 31423232 |
Disease Name: | Osteosarcoma |
Sample: | OS tissues and cell lines |
Dysfunction Pattern: | Interaction[c-Myc] |
Validated Method: | CCK8//qRT-PCR//Wound Healing Assay//Western Blot |
Description: | HOTTIP was demonstrated to be upregulated in OS tissues and cell lines.HOTTIP promoted cell migration and invasion by upregulating c-Myc in OS. The positive feedback loop formed by HOTTIP and c-Myc may contribute to OS progression, and HOTTIP may act as a therapeutic target for OS. |
Causality: | Yes |
Causal Description: | knockdown of HOTTIP inhibited OS cell migration, invasion and EMT, and suppressed c-Myc expression. In addition, overexpression of c-Myc increased HOTTIP expression and enhanced OS cell migration and invasion. |
Clinical-realted Application: | |
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